| First Author | Kim JS | Year | 2006 |
| Journal | Biochem Biophys Res Commun | Volume | 351 |
| Issue | 4 | Pages | 903-8 |
| PubMed ID | 17097608 | Mgi Jnum | J:116653 |
| Mgi Id | MGI:3694620 | Doi | 10.1016/j.bbrc.2006.10.135 |
| Citation | Kim JS, et al. (2006) Presenilin-1 inhibits delta-catenin-induced cellular branching and promotes delta-catenin processing and turnover. Biochem Biophys Res Commun 351(4):903-8 |
| abstractText | Although delta-catenin/neural plakophilin-related armadillo protein (NPRAP) was reported to interact with presenilin-1 (PS-1), the effects of PS-1 on delta-catenin have not been established. In this study, we report that overexpression of PS-1 inhibits the delta-catenin-induced dendrite-like morphological changes in NIH 3T3 cells and promotes delta-catenin processing and turnover. The effects of PS-1 on endogenous delta-catenin processing were confirmed in hippocampal neurons overexpressing PS-1, as well as in the transgenic mice expressing the disease-causing mutant PS-1 (M146V). In addition, disease-causing mutant PS-1 (M146V and L286V) enhanced delta-catenin processing, whereas PS-1/gamma-secretase inhibitors could block the formation of processed forms of delta-catenin. Together, our findings suggest that PS-1 can affect delta-catenin-induced morphogenesis possibly through the regulation of its processing and stability. |
